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The role of indoleamine 2,3-dioxygenase in a mouse model of neuroinflammation-induced depression

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The role of indoleamine 2,3-dioxygenase in a mouse model of neuroinflammation-induced depression. / Dobos, Nikoletta; de Vries, Erik F J; Kema, Ido P; Patas, Konstantinos; Prins, Marloes; Nijholt, Ingrid M; Dierckx, Rudi A; Korf, Jakob; den Boer, Johan A; Luiten, Paul G M; Eisel, Ulrich L M.

in: J ALZHEIMERS DIS, Jahrgang 28, Nr. 4, 2012, S. 905-15.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Dobos, N, de Vries, EFJ, Kema, IP, Patas, K, Prins, M, Nijholt, IM, Dierckx, RA, Korf, J, den Boer, JA, Luiten, PGM & Eisel, ULM 2012, 'The role of indoleamine 2,3-dioxygenase in a mouse model of neuroinflammation-induced depression', J ALZHEIMERS DIS, Jg. 28, Nr. 4, S. 905-15. https://doi.org/10.3233/JAD-2011-111097

APA

Dobos, N., de Vries, E. F. J., Kema, I. P., Patas, K., Prins, M., Nijholt, I. M., Dierckx, R. A., Korf, J., den Boer, J. A., Luiten, P. G. M., & Eisel, U. L. M. (2012). The role of indoleamine 2,3-dioxygenase in a mouse model of neuroinflammation-induced depression. J ALZHEIMERS DIS, 28(4), 905-15. https://doi.org/10.3233/JAD-2011-111097

Vancouver

Dobos N, de Vries EFJ, Kema IP, Patas K, Prins M, Nijholt IM et al. The role of indoleamine 2,3-dioxygenase in a mouse model of neuroinflammation-induced depression. J ALZHEIMERS DIS. 2012;28(4):905-15. https://doi.org/10.3233/JAD-2011-111097

Bibtex

@article{2ce3f55154bd4d9e86d3ede261c5aa2b,
title = "The role of indoleamine 2,3-dioxygenase in a mouse model of neuroinflammation-induced depression",
abstract = "Indoleamine 2,3-dioxygenase (IDO), an enzyme which is activated by pro-inflammatory cytokines, has been suggested as a potential link between neuroinflammatory processes in neurodegenerative diseases (like Alzheimer's disease) and depression. The present study aimed to determine whether neuroinflammation-induced increased IDO levels in the mammalian brain will lead to depressive-like behavior. Neuroinflammation was initiated in mice by a single intracerebroventricular injection of lipopolysaccharide (LPS). Cerebral inflammation was monitored 1, 2, 3 and 4 days after the injection with small-animal positron emission tomography (PET) using the inflammatory marker [(11)C]-PK11195. In the presence or absence of systemically applied 1-methyl-tryptophan (1-MT), a competitive IDO-inhibitor, we assessed the development of depressive-like behavioral symptoms in parallel with IDO expression and activity. The PK11195 PET signal reached a highly significant peak 3 days after LPS injection, while these animals displayed a significant increase of depressive-like behavior in the forced swim test compared to vehicle-injected animals. These findings were paralleled by a significant increase of IDO in the brainstem, and an increased kynurenine/tryptophan ratio in the serum. Moreover, we report here for the first time, that inhibition of IDO by 1-MT in centrally induced neuroinflammation under experimental conditions can prevent the development of depressive-like behavior.",
keywords = "Animals, Depression, Disease Models, Animal, Encephalitis, Indoleamine-Pyrrole 2,3,-Dioxygenase, Male, Maze Learning, Mice, Mice, Inbred C57BL, Tryptophan",
author = "Nikoletta Dobos and {de Vries}, {Erik F J} and Kema, {Ido P} and Konstantinos Patas and Marloes Prins and Nijholt, {Ingrid M} and Dierckx, {Rudi A} and Jakob Korf and {den Boer}, {Johan A} and Luiten, {Paul G M} and Eisel, {Ulrich L M}",
year = "2012",
doi = "10.3233/JAD-2011-111097",
language = "English",
volume = "28",
pages = "905--15",
journal = "J ALZHEIMERS DIS",
issn = "1387-2877",
publisher = "IOS Press",
number = "4",

}

RIS

TY - JOUR

T1 - The role of indoleamine 2,3-dioxygenase in a mouse model of neuroinflammation-induced depression

AU - Dobos, Nikoletta

AU - de Vries, Erik F J

AU - Kema, Ido P

AU - Patas, Konstantinos

AU - Prins, Marloes

AU - Nijholt, Ingrid M

AU - Dierckx, Rudi A

AU - Korf, Jakob

AU - den Boer, Johan A

AU - Luiten, Paul G M

AU - Eisel, Ulrich L M

PY - 2012

Y1 - 2012

N2 - Indoleamine 2,3-dioxygenase (IDO), an enzyme which is activated by pro-inflammatory cytokines, has been suggested as a potential link between neuroinflammatory processes in neurodegenerative diseases (like Alzheimer's disease) and depression. The present study aimed to determine whether neuroinflammation-induced increased IDO levels in the mammalian brain will lead to depressive-like behavior. Neuroinflammation was initiated in mice by a single intracerebroventricular injection of lipopolysaccharide (LPS). Cerebral inflammation was monitored 1, 2, 3 and 4 days after the injection with small-animal positron emission tomography (PET) using the inflammatory marker [(11)C]-PK11195. In the presence or absence of systemically applied 1-methyl-tryptophan (1-MT), a competitive IDO-inhibitor, we assessed the development of depressive-like behavioral symptoms in parallel with IDO expression and activity. The PK11195 PET signal reached a highly significant peak 3 days after LPS injection, while these animals displayed a significant increase of depressive-like behavior in the forced swim test compared to vehicle-injected animals. These findings were paralleled by a significant increase of IDO in the brainstem, and an increased kynurenine/tryptophan ratio in the serum. Moreover, we report here for the first time, that inhibition of IDO by 1-MT in centrally induced neuroinflammation under experimental conditions can prevent the development of depressive-like behavior.

AB - Indoleamine 2,3-dioxygenase (IDO), an enzyme which is activated by pro-inflammatory cytokines, has been suggested as a potential link between neuroinflammatory processes in neurodegenerative diseases (like Alzheimer's disease) and depression. The present study aimed to determine whether neuroinflammation-induced increased IDO levels in the mammalian brain will lead to depressive-like behavior. Neuroinflammation was initiated in mice by a single intracerebroventricular injection of lipopolysaccharide (LPS). Cerebral inflammation was monitored 1, 2, 3 and 4 days after the injection with small-animal positron emission tomography (PET) using the inflammatory marker [(11)C]-PK11195. In the presence or absence of systemically applied 1-methyl-tryptophan (1-MT), a competitive IDO-inhibitor, we assessed the development of depressive-like behavioral symptoms in parallel with IDO expression and activity. The PK11195 PET signal reached a highly significant peak 3 days after LPS injection, while these animals displayed a significant increase of depressive-like behavior in the forced swim test compared to vehicle-injected animals. These findings were paralleled by a significant increase of IDO in the brainstem, and an increased kynurenine/tryptophan ratio in the serum. Moreover, we report here for the first time, that inhibition of IDO by 1-MT in centrally induced neuroinflammation under experimental conditions can prevent the development of depressive-like behavior.

KW - Animals

KW - Depression

KW - Disease Models, Animal

KW - Encephalitis

KW - Indoleamine-Pyrrole 2,3,-Dioxygenase

KW - Male

KW - Maze Learning

KW - Mice

KW - Mice, Inbred C57BL

KW - Tryptophan

U2 - 10.3233/JAD-2011-111097

DO - 10.3233/JAD-2011-111097

M3 - SCORING: Journal article

C2 - 22112548

VL - 28

SP - 905

EP - 915

JO - J ALZHEIMERS DIS

JF - J ALZHEIMERS DIS

SN - 1387-2877

IS - 4

ER -